Fatty liver hemorrhage syndrome (FLHS) is a major cause of death in caged laying hens, associated with oxidative stress, hepatocyte injury, and inflammation. This study investigated the protective mechanisms of Lactiplantibacillus plantarum FRT4, focusing on its antioxidant and anti-inflammatory functions. Dietary supplementation with Lp. plantarum FRT4 significantly enhanced hepatic and ovarian antioxidant capacity, elevating levels of T-AOC, T-SOD, and GSH-Px, while upregulating gene expression of SOD1, SOD2, CAT, and GPX1. Concurrently, it reduced pro inflammatory cytokines such as TNF-α, IL-1β, and NLRP3, and downregulated mRNA levels of IL-1β, IL-6, and NLRP3, while promoting anti-inflammatory factors including IL-4 and IL-10. The intervention also remodeled gut microbiota composition, notably increasing beneficial genera like Prevotella and Alistipes, and influenced metabolic pathways related to tryptophan metabolism and FoxO signaling. Spearman correlation analysis confirmed close associations between microbial shifts and improvements in antioxidant and inflammatory indicators. Further mechanistic studies revealed that Lp. plantarum FRT4 modulates the FoxO/TLR-4/NF-κB signaling pathway through microbiota-mediated regulation, thereby mitigating oxidative damage and inflammatory responses. Ovarian function was likewise improved, as evidenced by increased levels of E2, FSH, and VTG. In summary, Lp. plantarum FRT4 alleviates FLHS by enhancing antioxidant defenses, suppressing inflammation, restructuring gut microbiota, and regulating the FoxO/TLR-4/NF-κB pathway, collectively supporting liver and ovarian health. Notably, these mechanisms share parallels with human metabolic associated fatty liver disease (NAFLD), suggesting that targeting the gut liver axis with probiotics could offer a promising strategy for ameliorating metabolic and inflammatory liver conditions in humans, warranting further investigation